The Circulating "Food" Supply and The Failed Internal Starvation Hypothesis
There are several recurring themes, mostly from low carb advocates of the "fat burning is best" bent, that keep ... well ... recurring! Perhaps foremost among these is this concept of "internal starvation". From Gary Taubes in Good Calories, Bad Calories:
"For the past century, the conspicuous alternative to the positive-caloric-balance hypothesis has always been, as Pennington, Astwood, and Hilde Bruch suggested, that obesity is caused by a defect in the regulation of fat metabolism. At the risk of repetition, it is important to say this is, by definition, a disorder of fat accumulation, not a disorder of overeating. For whatever reason , the release of fat or its combustion is impeded, or the deposition or synthesis of fat is promoted, as Astwood said, and the result is obesity. That in turn will cause a deficit of calories elsewhere in the body— Astwood’s “internal starvation”— and thus a compensatory hunger and sedentary behavior.
"In this hypothesis , obesity is another variation on the theme of insulin dysfunction and diabetes. In Type 1 diabetes, the cause is a lack of insulin. The result is an inability to use glucose for fuel and to retain fat in the fat tissue, leading to internal starvation, as Astwood put it, excessive hunger, and weight loss. In obesity, the cause is an excess of insulin or an inordinate sensitivity to insulin by the fat cells; the result is an overstock of fuel in the adipose tissue and so, once again, internal starvation. But now the symptoms are weight gain and hunger. In obesity, the weight gain occurs with or without satisfying the hunger; in Type 1 diabetes, the weight loss occurs irrespective of the food consumed.
"This half century of research unequivocally supported the alternative hypothesis of obesity. It established that the relevant energy balance isn’t between the calories we consume and the calories we expend, but between the calories— in the form of free fatty acids, glucose, and glycerol— passing in and out of the fat cells. If more and more fatty acids are fixed in the fat tissue than are released from it, obesity will result. And while this is happening, as Edgar Gordon observed, the energy available to the cells is reduced by the “relative unavailability of fatty acids for fuel.” The consequence will be what Stephen Ranson called semi-cellular starvation and Edwin Astwood, twenty years later, called internal starvation. And as this research had now made clear, the critical molecules determining the balance of storage and mobilization of fatty acids, of lipogenesis and lipolysis, are glucose and insulin— i.e., carbohydrates and the insulin response to those carbohydrates.The less ballyhooed paper (Effects of Diet Composition on Postprandial Energy Availability during Weight Loss Maintenance) to come out of the Ebbeling/Ludwig energy expenditure study, was one putting forth, yet again, a "circulating energy" hypothesis for why carbs and glycemic index alter hunger and eating behavior. I discussed this paper in more depth previously: The Myth of Starving Cells II and NEFA Levels Again
Here are glucose (mg/dL, top), NEFA (mEq/L or mmol, middle), and Energy Available (kcal/L, bottom). I stretched the EA plot a bit vertically for detail, and horizontally to match up the time scale.
What jumped out at me the first time I read this paper was the axis units on EA = kcal/L. With the exception of about 30 minutes -- between 15 and 45 minutes after the ~650 cal meal, the EA remains roughly between 4 kcal/L and 5 kcal/L, or the total energy in 5 liters of blood is between perhaps 20 and 25 kcal. A kcal is a single Calorie. Five -- 5! -- Calorie total swing.
So I got to wondering how these shook out between the energy substrates. I didn't include the ketone plot, because it constitutes only 1-2% of circulating energy anyway, but I used the calculations from the paper to look at the relative EA at several time points. I wanted to get a better feel for which substrate is contributing what. Their factors:
Glucose (mg/dL) * 0.04
FFA (mEq/L) * 2.434
BHB (mmol/L) * 0.437
So again, not all time points were included here, but Total EA remains between 4-5 kcal/L except for the 30 minute spike. While the ratios of circulating substrates were different for the low carb, we see that the least glucose contributes is still over 70% of the Total EA. Immediately after the High GI LF meal, glucose makes up over 90% of the Total EA.
- Normal fasting glucose of 80 mg/dL and fatty acids of 0.4 mmolar, gives a 77% glucose, 23% FFA split of circulating EA of just under 4.2 kcal/L.
- If we increase glucose just 50% to 120 mg/dL, and suppress fatty acids to 25% of baseline at 0.1 mmolar, glucose now becomes 95% of about 5 kcal/L
- To get a 50-50 split of EA between glucose and FFA, one has to go with quite a low glucose of 60 mg/dL and a fairly abnormally high FFA of 1.0 mmolar. In other words, the nature of the calories the cells have access to always favors glucose.
A Few Concluding Comments:
Circulating Calories/Substrates and Carb vs. Fat Burning:
It Appears to be Impossible to Starve Cells of Fat:
Based on the hundreds of glucose and NEFA levels and profiles that I've seen in various studies, coupled with the background physiology, it is fair to say that glucose levels are much more tightly regulated. There is also a pretty definitive minimum (that can be pushed lower in ketosis) for glucose, whereas there does not appear to be a lower danger limit for NEFA. If such exists, it is apparently near impossible to achieve either with diet or drugs. I have seen NEFA suppressed below 0.07 mmolar (using an exogenous agent) with no indication of safety concerns in the experimental protocol. Can you imagine a study allowing people to be given something to drop their blood glucose to 30 mg/dL? This level of NEFA is more like dropping glucose to 10!
Hunger Tracks with NEFA Levels:
The tracking of hunger with EA is most similar to the profile for NEFA such that: low NEFA = low hunger, high NEFA = high hunger. This is in direct opposition with the notion of "starving cells". As I've discussed, non-adipose, aka ectopic, cells receive higher than normal NEFA delivery (often resulting in fat accumulation) when the circulating EA from fatty acids is high as in obesity and diabetes. But this puts the kibosh on the whole insulin → low NEFA → hunger → eating more. Hyperphasia (overeating) has been shown experimentally when glucose levels dip too low, however.
One scientifically ignorant person "vindicating" the distortions and mistruths of another scientifically ignorant person.
Zoe Harcombe spoke at Barry Groves funeral ...
Barry Groves: Homo Carnivorus - What We Are Designed to Eat
"When Oxfordshire Cotswolds native Dr. Barry Groves and his wife Monica decided to start on a low-carb, high-fat diet beginning in 1962, all of his friends and family thought he was crazy. But when this nutritional scientist Ph.D. lost weight and greatly improved his health by eating supposedly-forbidden foods like butter, full fat meats and cheeses and lard while eschewing blood sugar-spiking carbage foods like bread, pasta and rice, Dr. Groves was the one who had the last laugh. It allowed him to live a long and healthy robust life with over a half century of enjoyable low-carb, high-fat living as one of the UK’s strongest advocates for this healthy lifestyle change. Dr. Groves passed away last night, April 29, 2013 at the age of 77."
A "long(!) and healthy robust life" that ends at the age of 77(!) in the 21st century???
Lutz did not advocate an extremely low carb Jimmy Moore-type diet.
A ketogenic level of carb restriction was not necessary to achieve the benefits [as Lutz saw them] of low-carb nutrition. We know the potential pitfalls:
"...in the absence of dietary carbohydrates, lipolysis of stored triglycerides and the oxidation of fatty acids increase and ketone bodies accumulate. A carb-free diet also is generally associated with an accelerated breakdown of dietary and tissue protein, loss of cations (especially sodium) and dehydration. [HOWEVER!:] These effects produced by low-carb diets or by fasting can be prevented by the daily ingestion of 50 to 100g of carbs." [National Research Council. Recommended Dietary Allowances. 10th ed. National Academy Press. p.41]
In Leben Ohne Brot(1967)—[i.e., "Life Without Bread"], Lutz advised ~72g/day of carbs, which is right in the middle of that 50 to 100g range cited above that prevents all those listed unwelcome side effects produced by greater carb restriction.
As to whether such a moderate and non-extreme 72g/day low-carb diet merits being called "sick"? Well, this is, shall we say, an unscientific appraisal, and in this department opinion divides.
"With a doctorate in nutritional science from the American distance learning university, Trinity College & University, (NOT the Spanish diploma mill with a similar name) gained from 20 years’ research experience and a 60.000-word dissertation on the Politics of the Fluoridation of Public Water Supplies (Commercial version), he now divides his time between writing and giving talks to Womens’ Institutes, Probus, and other groups and as a guest lecturer on cruise liners. "
I am not sure if that is the Trinity in West Hartford CT, but online PhD = red flag. It wasn't a research PhD, and it was about flouridation of water mostly politics. Scroll down for the TOC here: http://www.second-opinions.co.uk/fluoride_book.html#.VN-QdvnF_kI
I don't mean to imply that LC is necessarily killing these folks, just that with Groves, his diet may well not have been the healthiest choice for him. I don['t know what his cholesterol levels were, but he was a THINCS founder.
Somone mentioned Kendrick. That's him (blue shirt) and 3 other THINCers at a recent event. I'd take these folks more seriously if they weren't all so inflamed looking as they lecture everyone else about how carbs cause inflammation and how healthy they are on their LCHF diets.
For someone obsessed with the perceived conflicts of others she appears to have been hoist by her own petard!
Just who and in what capacity are Harcombe and DiNicolantonio affiliated with on any given day?
Columbus Publishing Ltd and Columbus Digital Services Ltd are the publishing company of the hard books and kindle downloads (obesity epidemic, harcombe diet, why do we overeat).
She is a majority or equal shareholder in all as far as I can tell along with her husband. Here are indicative accounts http://companycheck.co.uk/director/907354579
Not multi million pound businesses, but without business which would benefit massively from - and have argued for - vindication of sat fat.
DiNicholantonio is a co-author of the paper - could he not have advise her? (especially since this is the second paper he has co-authored and hence must be aware she had made no declaration previously)
Equally, who peer reviewed it?
Because they are also supposed to flag up concerns about undeclared competing interests too.
Unfortunately I can't find a public link to their COI disclosure form. One would think these things would be pretty specific to list what should be disclosed.
(1) Here is the BMJ Group Competing Interest policy: http://www.bmj.com/sites/default/files/BMJ_Group_policy_on_declaration_of_interests.pdf
Open Heart is a BMJ Group publication. This brings DiNicolantonio into question as well as Harcombe, as Zoe is "friends" with DiN having authored papers with him before. He is an editor and co-author on her paper. His position as Associate Editor needs to be disclosed IMO.
(2) I think I tracked down what you're talking about vis a vis the journal: http://www.zoeharcombe.com/2015/02/competing-interest/
But I don't see any statement with the article. Don't really know what that means.
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